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1 Dept of Cell and Molecular Physiol CB #7545, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
2 Cell and Molecular Physiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, United States
* To whom correspondence should be addressed. E-mail: sfellner{at}med.unc.edu.
We have previously shown that in afferent arterioles, angiotensin II (Ang II) results in activation of the inositol trisphosphate receptor (IP3R), activation of adenine diphosphoribose (ADPR) cyclase, and amplification of the initial IP3R stimulated release of cytolsolic Ca2+ ([Ca2+]i ) from the sarcoplasmic reticulum (SR). The response of the ryanodine receptor (RyR) to local increases in [Ca2+]i is defined as calcium induced calcium release (CICR). To investigate if Ca2+ entry via voltage-gated channels (VGCC) can stimulate CICR, we treated fura-2 loaded, freshly isolated afferent arterioles with KCl (40 mM). In control arterioles, [Ca2+]i increased by 165 ± 10 nM. Locking the RyR in the closed position with ryanodine (100 µM) inhibited the [Ca2+]i response by 59% (P< 0.01). 8-Br cADPR, a specific blocker of the ability of cADPR to sensitize to RyR to Ca2+, caused a 43% inhibition. We suggest that the lower inhibition by 8-Br cADPR (P = 0.02, ryanodine vs. 8-Br cADPR) represents endogenously active ADPR cyclase. Depletion of SR Ca2+ stores by inhibiting the SR Ca2+ - ATPase with cyclopiazonic acid or thapsigargin, blocked the [Ca2+]i responses to KCl by 51% (P NS vs. ryanodine or 8-Br cADPR). These data suggest that about half of the increase in [Ca2+]i induced by KCl is accomplished by activation of CICR through the ability of entered Ca2+ to expose the RyR to high local concentrations of Ca2+ and that endogenous cADPR contributes to the process.
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